Corrected Sinus Node Recovery Time Research Articles

Electrophysiologic effects of intravenous xamoterol in patients with sinus node dysfunction

The electrophysiologic effects of xamoterol were studied in ten patients with electrophysiologic evidence of sinus node dysfunction. A significant shortening of mean sinus cycle length, maximal corrected sinus-node recovery time, and the mean of the three longest corrected sinus-node recovery times was observed after intravenous administration of 0.1 mg/kg of xamoterol. The atrioventricular (AV) conduction time and the effective and functional refractory periods of the AV node were shortened as the effective refractory period of the atrium. These effects suggest that xamoterol could be tried safely for the treatment of patients with moderate symptoms due to sinus-node disease.

Electrophysiologic studies of the heart in patients with rheumatoid arthritis

We investigated the electrophysiological properties of the heart in patients with definite or classical rheumatoid arthritis using programmed electrical stimulation techniques. Twelve patients with rheumatoid arthritis and without evidence of organic heart disease or arrhythmia detectable with serial electrocardiograms and 24-hour ambulatory electrocardiographic monitoring were compared with 12 control subjects. Stimulation was performed from the high right atrium and right ventricular apex at a drive cycle length of 600 msec and the recording sites included high right atrium, atrioventricular junction and distal coronary sinus. There was no statistically significant difference in the corrected sinus node recovery time between the study and control group of patients. Similarly, no differences from normal were found in the AH and HV intervals or in the atrial and ventricular refractoriness, whereas the atrioventricular nodal effective refractory period was higher in patients with rheumatoid arthritis, compared with the control group (338 ± 38 vs 286 ± 29, P < 0.02). The atrial conduction time during basic cycle length had a tendency to increase from high right atrium to atrioventricular junction in the study group and reached statistical significance from high right atrium to coronary sinus (92 ± 15 vs 74 ± 14, P < 0.05). Electrophysiologic differences between the study and control patients also included a greater increase in maximal intraatrial (40 ± 13 vs 27 ± 16, P < 0.05) and interatrial conduction delay (54 ± 16 vs 31 ± 12, P < 0.01) of early premature stimuli in patients with rheumatoid arthritis. In addition atrial arrhythmias were induced in 3 patients with rheumatoid arthritis but in no control patient. The clinical importance of these findings is uncertain. Nevertheless, our data suggest that abnormalities in atrial conduction time may be present in patients with rheumatoid arthritis and predispose to the initiation of atrial tachyarrhythmias.

Electrophysiological evaluation of the sinus node in patients with atrioventricular and/or intraventricular conduction defects

The authors evaluated retrospectively sinoatrial conduction time (SACT), sinus node recovery time (SNRT), and corrected sinus node recovery time (CSNRT) in 272 patients with atrioventricular and/or intraventricular conduction defects without evidence of overt sinus node dysfunction. The study was designed to determine the prevalence of electrophysiologic sinus node abnormalities in patients with overt atrioventricular and/or intraventricular conduction defects. One or more sinus node electrophysiological abnormalities were observed in 133 cases (48.9%). There was a significant prevalence of electrophysiologic sinus node abnormalities only in patients older than 71 years of age. The data suggest that the involvement of the specialized conduction system is much more diffuse than one might expect simply observing the single recorded ECG defect and that the prevalence of associated defects of the conduction system increases with increasing age of patients.

Effect of nifedipine on the sick sinus syndrome.

The effect of nifedipine (N) on sinus node (SN) function was studied in 15 patients (9 males, 6 females) sixty-two to seventy-six (mean 68.1 +/- 11) years old, with sick sinus syndrome (SSS). SSS was characterized electrophysiologically by a prolonged corrected sinus node recovery time (CSNRT greater than 535 msec) and/or prolonged sinoatrial conduction time (SACT greater than 125 msec), assessed by applying premature atrial stimulation. Ten mg N was given sublingually, and CSNRT and SACT were again evaluated sixty minutes after N administration, and again ten minutes after 1.5 mg atropine (A) was given IV. Heart rate increased significantly after N (p less than 0.005), systolic blood pressure (SBP) diminished significantly (p less than 0.005), and CSNRT and SACT shortened significantly (p less than 0.005, p less than 0.005) and became normal in 7 and 5 patients respectively. After A administration, a further significant increase of heart rate (p less than 0.005) and decrease of CSNRT (p less than 0.005) and SACT (p less than 0.005) were observed. CSNRT and SACT became normal in 8 and 7 patients respectively. SBP remained stable.

Cardiac electrophysiologic properties of intravenous isradipine in patients with sick sinus syndrome

Isradipine is a new dihydropyridine calcium antagonist with powerful vasodilating properties. Although therapeutic concentrations do not affect myocardial contractility in vivo, in vitro studies have demonstrated a negative chronotropic action with only minor dromotropic influence. In humans with normal sinus and atrioventricular node function, even in the presence of beta-blockade, such a negative chronotropic effect could not be proved. No data are available on the effects of isradipine on a compromised sinus node. Therefore, the effect of intravenous isradipine at 0.3 μg/kg/minute for 30 minutes was studied in seven patients with the clinical signs of a sick sinus syndrome. Mean arterial blood pressure decreased from 126 ± 21 to 113 ± 15 mm Hg (p <0.05). Spontaneous sinus cycle length decreased from 969 ± 22 to 843 ± 161 msec (p <0.05). Changes in sinoatrial conduction time, sinus node recovery time, and corrected sinus node recovery time were not significant. Changes in atrioventricular node functional refractory period, the atrial-His interval, the His-ventricle interval, and Wenckebach point were not significant. Also, effective. Also, effective refractory periods of atrium and ventricle, and QRS duration changed but not significantly. The QT interval decreased (419 ± 45 to 405 ± 44 msec; p <0.05), and there was a slight (not significant) increase of QTc interval (429 ± 41 to 443 ± 37 msec; not significant). It is concluded that isradipine in hemodynamically effective doses has no depressant effect on sinus and atrioventricular node function in patients with sick sinus syndrome.

Asystole with Syncope Secondary to Hyperventilation in Three Young Athletes

We describe three athletes who had syncope after (case 1) or during (cases 2, 3) hyperventilation. During the episode, ECG showed prolonged sinus arrest. Clinical data and noninvasive investigations were normal and the phenomenon was not reproducible. Electrophysiological study after autonomic blockade allowed a prolonged intrinsic heart rate in case 1, and abnormal corrected sinus node recovery time in cases 1 and 2. During follow-up, symptomatic sinus arrest provoked by deep inspiration occurred in case 3. These cases document prolonged asystole of unknown etiology, secondary to hyperventilation, and probably caused by different vagally-mediated mechanisms.

Reliability of Transesophageal Pacing in the Assessment of Sinus Node Function in Patients with Sick Sinus Syndrome

The purpose of this study was to find out whether transesophageal pacing could be utilized for assessment of sinus node function in patients with sick sinus syndrome (SSS). In 17 patients with SSS (study group) we compared the results of sinus node tests obtained both in the basal state and after pharmacological autonomic blockade by endocavitary stimulation and, 24 hours later, by transesophageal pacing. In another group of 17 patients with SSS (control group), we compared the results obtained by two endocavitary studies. In "study group", sinus cycle length (SCL) and corrected sinus node recovery time (CSRT) did not show significant differences between the two studies both in the basal state and after autonomic blockade, whereas sinoatrial conduction time (SACT) was more prolonged during esophageal pacing (P less than 0.01). In "control group", sinus node measures did not show significant differences between the two studies. In the "study group," the following coefficients of correlation were obtained in the basal state; SCL, r = 0.65, CSRT, r = 0.57, SACT, r = 0.52 and after autonomic blockade: SCL, r = 0.95, CSRT, r = 0.62 and SACT, r = 0.53. In the basal state, the correlation for SCL and CSRT between the two studies was lower in the "study group" than in the "control group" (P less than 0.05), whereas after autonomic blockade the correlation for sinus node measures did not show significant differences between the two groups of patients. These data suggest that transesophageal study influences the autonomic tone regulating the sinus node; however, it is not responsible for important variations in sinus node measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic evaluation of intravenous nicardipine in man

The acute electrophysiological effects of intravenous nicardipine (0.014 mg/kg per min for 5 minutes) were studied in 12 subjects with estimated normal sinus node functions and atrioventricular conduction parameters. The most important effects were sinus cycle length shortening, increase of corrected sinus node recovery time and reduction of effective and functional refractory period of the atrioventricular node. Sinuatrial conduction time, atrial refractory periods, intranodal conduction, bundle branch refractoriness and ventricular refractoriness were unchanged. Systolic and diastolic blood pressure was reduced. The clinical implications of these properties of the drug are discussed and compared with those of verapamil, diltiazem and nifedipine.

Sinus node function and protamine sulfate

This report analyzes the effects of protamine sulfate (PS) on the heart rate and sinoatrial node function in dogs anesthetized with diazepam, fentanyl, and pancuronium bromide, and subjected to different modalities of extracorporeal circulation (ECC). All groups were given 3 mg/kg of heparin sodium and 5 mg/kg of PS. The sinus node function was evaluated by means of sinoatrial conduction time (SACT), absolute sinus node recovery time (SNRTa), and corrected sinus node recovery time (SNRTc). The spontaneous heart rate (HR) of the animals was also analyzed. Under the experimental conditions established in this study, the intravenous administration of a bolus of PS produced a decrease in the HR in all the groups, regardless of the type of ECC used. The modifications in the conduction and recovery times of the sinus node by PS did not correlate with those of the heart rate; the sinoatrial conduction time increased in groups subjected to ECC, while the absolute and corrected recovery times of the sinus node were prolonged only in the group that underwent rapid rewarming.

The electrophysiologic effects of enoximone in patients with preexisting ventricular tachyarrhythmias

Electrophysiologic and hemodynamic effects of intravenous enoximone were studied in 15 male patients, mean age 62.2 years, with New York Heart Association classes II to IV congestive heart fallure (coronary artery disease in 10 and idlopathic dllated cardiomyopathy in five patients; mean ejection fraction, 0.19). All patients had spontaneous ventricular tachyarrhythmias: eight had sustained ventricular tachycardia (VT), one had ventricular fibrillation, and six had nonsustained VT. Hemodynamic and electrophysiologic parameters including VT induction were determined before and during an intravenous infusion of enoximone. The cardiac index increased (2.49 ± 0.89 to 2.96 ± 0.78), and the pulmonary capillary wedge pressure decreased (22.4 ± 13.2 to 10.0 ± 9.0) after enoximone per predefined protocol endpoints. There was a significant decrease in spontaneous sinus cycle length, corrected sinus nodal recovery time, AH interval during atrial pacing, shortest cycle length at which 1:1 atrioventricular nodal conduction occurred, and refractory periods of the atrium, ventricle, and atrioventricular node. Enoximone did not alter the cycle length of induced VT, and there was no consistent change in the number of extrastimuli required for VT induction. A baseline 24-hour ECG recording was obtained on 14 patients (while recelving a long-term antiarrhythmic drug regimen, if needed) and repeated after 1 week and 1 month of oral enoximone therapy. There was no significant increase in the number of premature ventricular complexes per hour or VT episodes per 24 hours after 1 week or 1 month of therapy with enoximone. However, if four patients who received amiodarone and may not yet have reached steady state were excluded from analysis, there was a significant increase in the frequency of premature ventricular complexes per hour 1 month after initiation of enoximone. We conclude that intravenous enoximone reduces pulmonary capillary wedge pressure and increases cardiac output in most patients. Intravenous enoximone in doses sufficlent to have hemodynamic effects shortens atrial, ventricular, and atrioventricular nodal refractoriness and decreases AV nodal conduction time but has no consistent effect on VT induction or VT cycle length. The frequency of spontaneous ventricular ectopy may increase in some patients after oral enoximone, but its clinical significance is undefined. Enoximone may be administered cautiously to patients with congestive heart fallure and preexisting ventricular tachyarrhythmias.

CARDIAC CONDUCTION INTERACTIONS OF PROPRANOLOL AND VERAPAMIL WITH HALOTHANE IN PENTOBARBITONE-ANAESTHETIZED DOGS

We have studied the effects of propranolol 0.25 mg kg-1 and verapamil 0.075 mg kg-1 on cardiac conduction and refractoriness in 21 dogs anaesthetized with pentobarbitone 30 mg kg-1 using His bundle electrocardiography and programmed stimulation. After baseline studies under pentobarbitone and halothane (1.3 MAC) anaesthesia, the dogs were allocated randomly to two groups: group 1 received verapamil followed by propranolol; group 2 received propranolol followed by verapamil; the drugs were given in a continuous infusion over 10 min. The atrial-His (AH) interval, the atrioventricular node effective (AVERP), and functional (AVFRP) refractory periods, were prolonged by verapamil in both groups, but not the His-ventricle (HV) interval or the ventricular effective refractory period (VERP). AVFRP and VERP were prolonged by propranolol in both groups. Corrected sinus node recovery times were normal after each drug. Heart rate and the rate required to produce Wenckebach were decreased by each drug. The combination of verapamil and propranolol during halothane anaesthesia in dogs has significant cardiac conduction effects; however, no spontaneous AV block occurred during the study.

Effects of Diproteverine, a New Calcium Antagonist on Sinoatrial Node and Atrioventricular Conduction in Conscious Unsedated Dogs

The electrophysiologic effects of diproteverine were studied in the conscious nonsedated chronically instrumented dog. Diproteverine at 0.25-0.75 mg/kg (i.e., at plasma levels within the assumed therapeutic range) dose-relatedly decreases heart rate, increases corrected sinus node recovery time, and decreases Wenckebach point. These effects are observed at plasma levels ranging between 16.2 +/- 4.1 and 144.7 +/- 12.5 ng/ml. After cholinergic blockade with N-methylscopolammonium, diproteverine lowers heart rate (greater than or equal to 0.25 mg/kg), increases corrected sinus node recovery time, and decreases Wenckebach point (greater than or equal to 0.5 mg/kg). After propranolol, diproteverine only significantly reduces corrected sinus node recovery time 5 min after the third administration (0.75 mg/kg). After pharmacologic autonomic blockade by N-methylscopolammonium propranolol combination, diproteverine lowers intrinsic heart rate (greater than or equal to 0.25 mg/kg) and Wenckebach point (greater than or equal to 0.5 mg/kg). Diproteverine does not modify mean blood pressure. These results show that diproteverine administered with and without pharmacologic autonomic blockade in the conscious dog causes dose-related depressant effects on sinus node function and atrioventricular conduction without producing significant vasodilatation.

Functional abnormalities of the conduction system in children with an atrial septal defect

We performed an electrophysiologic study in 40 children with an atrial septal defect and analyzed their pre- and postoperative electrocardiograms and 24-hour Holter recordings. The electrophysiologic study showed a prolonged corrected sinus node recovery time in 83% and an abnormal sinuatrial conduction time in 25% of the children. An early Wenckebach response to atrial pacing was seen in 18%. Sixteen percent had a prolonged atrial conduction time. The atrial functional refractory period was abnormal in 35%. Two children developed nonsustained supraventricular tachycardia during the electrophysiologic study. The preoperative electrocardiogram showed first-degree atrioventricular block in 15% of the children; prolonged periods of accelerated atrial rhythm were found in 35% of the preoperative 24-hour Holter recordings. The incidence of first-degree atrioventricular block and accelerated atrial rhythm decreased postoperatively. We could not find a significant correlation between age or shunt size and the presence of electrophysiologic abnormalities or arrhythmias. These results indicate that the sinus node, atrioventricular node and atrial myocardium show some degree of dysfunction in patients with an atrial septal defect. An early operation may prevent further progression of electrophysiologic abnormalities and the development of symptomatic arrhythmias.

Electrophysiologic consequences of the arterial switch repair of d-transposition of the great arteries

Electrophysiologic studies were performed at 12.7 ± 4 months postoperatively in 20 patients who had the arterial switch repair at 1 to 120 days (mean 13 ± 26 [SD]) for d-transposition of the great arteries. Preoperative electrocardiograms (ECGs) at rest revealed an ectopic atrial rhythm in one patient. Postoperative rest ECGs revealed transient postoperative ectopic atrial or junctional rhythms in two patients, intermittent ectopic atrial rhythms in two and right bundle branch block in nine with a normal QRS axis. In addition, ambulatory monitor recordings revealed infrequent premature ventricular complexes in five patients. Catheter endocardial mapping revealed sinus rhythm in 18 patients and ectopic atrial rhythm in 1 patient. Atrial activation after the switch repair was comparable with normal atrial activation. Activation of all low atrial sites was significantly earlier after the switch repair than after the Mustard repair.Mild abnormalities of sinus node function were present and consisted of slight prolongation of corrected sinus node recovery time in six patients and slightly increased sinoatrial conduction time in four. The ratio of sinus node recovery time to sinus cycle length was normal in all 20 patients. Atrial effective and functional refractory periods were normal ia all patients and no atrial arrhythmias could be induced by programmed stimulation. Atrioventricular (AV) node conduction was excellent with normal AV node effective and functional refractory periods. The only electrophysiologic abnormality of His-Purkinje function was distal right bundle branch block in nine patients. Programmed stimulation of the ventricle produced repetitive ventricular responses in four patients: bundle branch reentry in three and intraventricular reentry in one. In summary, electrophysiologic abnormalities after the arterial switch repair were mild and infrequent.

Electrophysiologic and hemodynamic effects of chronic oral therapy with the α2-agonists clonidine and tiamenidine in hypertensive volunteers

Clonidine can produce symptomatic sinus bradycardia or atrioventricular (AV) block in some patients. Electrophysiologic studies have been performed after intravenous clonidine in patients showing such side effects; these have demonstrated variable depression of sinus and AV nodal function. We have evaluated the electrophysiologic and hemodynamic effects of chronic oral treatment with either clonidine (0.2 to 0.5 mg every 12 hours; n = 7) or another centrally active alpha 2-agonist, tiamenidine (0.5 to 1.5 mg every 12 hours; n = 7), in otherwise healthy hypertensive human volunteers. At dosages that modestly lowered diastolic blood pressure, both agents significantly slowed sinus rate and increased the atrial pacing rate producing AV nodal Wenckebach. Clonidine also significantly increased corrected sinus node recovery time and lowered cardiac output while similar (but statistically insignificant) trends were seen with tiamenidine. We conclude that chronic oral treatment with these alpha 2-agonists depresses sinus and AV nodal function in virtually all subjects, including those without manifest conduction system disease.

Effects of the volatile anesthetic agents on sinus node function and atrioventricular conduction in dogs: A comparison with chloralose anesthesia

The effects of equipotent concentrations (1.5 times minimum alveolar concentration) of the inhalational agents halothane, enflurane, and isoflurane on sinus node function, and atrioventricular (A-V) conduction and refractoriness were compared with chloralose anesthesia in 49 mongrel dogs. Sinus node function was assessed using corrected sinus node recovery time. Atrial-His and His-ventricular conduction times were measured at paced heart rates of 150, 180, and 200 beats/min, and A-V refractoriness was assessed by Wenckebach periodicity. There was no evidence that sinus node function was impaired by any of the inhalational agents. Enflurane anesthesia was associated with a significant prolongation of atrial-His conduction at paced heart rates of 180 and 200 beats/min when compared to chloralose anesthesia and the other two inhalational agents ( P < .001). Atrioventricular refractoriness was impaired by enflurane ( P < .001) and halothane ( P < .05), but not isoflurane, when compared with chloralose anesthesia. Ventricular-His conduction was not altered by any of the agents. The authors conclude that enflurane is associated with a greater impairment of AN conduction and refractoriness than halothane or isoflurane, and that these changes are related to the anesthetic agent .and not the anesthetic state.

Direct and autonomically mediated effects of oral flecainide

This study was undertaken to determine if oral flecainide exerts autonomically mediated actions in addition to its direct depressant effect. Electrophysiologic studies were performed twice in each of 15 patients (mean age 59 years) with normal resting and intrinsic heart rate and normal A-H interval. In the first study, the variables of sinus node and atrioventricular node were evaluated both in the basal state and after autonomic blockade (propranolol 0.2 and atropine 0.04 mg/kg). Oral flecainide was administered for 4 to 5 days (200 to 250 mg daily) and the study was then repeated using the same methods. From comparison of data obtained in the 2 studies in the basal state, the overall effect of flecainide was evaluated and by comparing those obtained after autonomic blockade, the direct action of the drug was assessed. The overall effect of flecainide on sinus node was slight; sinus cycle length, corrected sinus node recovery time and sinoatrial conduction time did not change significantly after the drug. In contrast, after autonomic blockade the variables of sinosal automaticity were increased significantly (p < 0.01). Flecainide significantly prolonged the atrioventricular node variables both in the basal state and after autonomic blockade (p < 0.01), but the degree of increase was more marked after autonomic blockade (p < 0.05). These data show dual effects of oral flecainide: a direct depressant action and an autonomically mediated opposing action, likely of vagolytic type.

Electrophysiologic properties of intravenous isradipine in persons with normal sinus node and atrioventricular nodal function

Isradipine (PN 200-110) is a new dihydropyridine calcium entry blocker with powerful vasodilating properties. Plasma concentrations obtained after commonly used dosage do not decrease myocardial contractility. However, in vitro studies have demonstrated negative chronotropic action with only minor dromotropic influence. Therefore, the electrophysiologic properties of intravenous isradipine 0.3 μg/kg for 30 minutes in persons with normal sinus and atrioventricular nodal function were investigated. There were no unwanted side effects. Mean blood pressure decreased slightly, but not significantly (107 ± 19 to 100 ± 9 mm Hg). Sinus cycle length decreased from 798 ± 176 to 730 ± 163 msec (p <0.01). The atrioventricular nodal functional refractory period decreased from 418 ± 40 to 399 ± 47 (p <0.05) and the atrial His interval decreased from 95 ± 20 to 91 ± 20 (p <0.01). The His ventricle interval, corrected sinus node recovery time, Wenckebach cycle length, and QRS duration remained unchanged. The QT c was prolonged from 417 ± 39 to 427 ± 40 (p <0.01). It was concluded that isradipine has no depressant effect on normal sinus and atrioventricular node function in humans and is well tolerated. The electrophysiologic effects seem to be the results of enhanced sympathetic tone provoked by peripheral vasodilatation.

Assessment by autonomic blockade of age-related changes of the sinus node function and autonomic regulation in sick sinus syndrome

Age-related changes of the sinus node (SN) function and the autonomic influence on the SN function were evaluated in 65 patients with sick sinus syndrome (range 14 to 84 years). Heart rate (HR), corrected SN recovery time and sinoatrial conduction time were measured before (basic) and after (intrinsic) autonomic blockade (propranolol 0.2 mg/ kg plus atropine 0.04 mg/kg intravenously). Percent of autonomic chronotropies of the SN function were calculated by the following formulas: (1) — (intrinsic HR — basic HR/intrinsic HR) × 100; (2) (intrinsic corrected SN recovery time — basic corrected SN recovery time/intrinsic corrected SN recovery time) × 100; (3) (intrinsic sinoatrial conduction time — basic sinoatrial conduction time/intrinsic sinoatrial conduction time) × 100. Basic HR, basic corrected SN recovery time and baste sinoatrial conduction time did not vary with age. Intrinsic HR decreased with age, but this correlation was weak (r = −0.54, p < 0.001). Intrinsic corrected SN recovery time and intrinsic sinoatrial conduction time tended to increase with age (r = 0.26, p < 0.05; r = 0.29, p < 0.05, respectively). Percent chronotropies of HR, corrected SN recovery time and sinoatrial conduction time were negative values in younger patients and positive values in elderly patients; they correlated positively with age (r = 0.59, p < 0.001; r = 0.60, p < 0.001; r = 0.43, p < 0.001, respectively). Thus, the basic SN function did not change with age, while the intrinsic SN function deteriorated with age. In the SN function, parasympathetic tone was predominant in younger patients and sympathetic tone was predominant in elderly patients with sick sinus syndrome. Age-related enhancement of sympathetic tone may mask the age-related deterioration of the intrinsic SN function.

Diagnostic value pharmacological autonomic blockade in patients with suspected sick sinus syndrome.

The study comprised 67 subjects, mean age 43.7 years, with suspected sick sinus syndrome, in whom rapid atrial pacing before and after combined atropine and propranolol was performed by Narula's method. Three groups were formed: group I--with normal sinus node recovery time (SNRT) and corrected sinus node recovery time (CNRT) before and after the autonomic blockade; group II--with functional disorders of the sinus node and group III--with intrinsic sinus node dysfunction. After autonomic blockade in groups I and II mean SNRT, CNRT, post-stimulation cycle lengths (except No. 2 and Nos. 5, 6, 10, respectively) shortened, whereas HR rose. In contrast, in group III mean SNRT, CNRT, post-stimulation cycle lengths (Nos. 1, 2, 6, 10) and HR increased. Significant differences in post-stimulation cycle lengths were observed between groups I and III as well as groups II and III. In conclusion, rapid atrial pacing after combined atropine and propranolol helps us to diagnose latent sick sinus syndrome and extrinsic sinus node dysfunction more precisely, and significant differences in post-stimulation cycle lengths between the groups confirm diagnostic value.